week 7 part 1

chapter 4!!!!!!!!

what is the receptor of proprioceptive information

cerebellum

sensory cortex is composed of…

1. primary sensory cortex (S1) → where sensory information from the outside enters by way of the spinal cord and brainstem

2. secondary sensory cortex (S2) → analyses shape, location in space and movement

3. tertiary sensory cortex/ parieto-temporo-occipital association area (S3) → links sensory information to visual or auditory information → links to events from the past to form a concept

   !! not only sensation but also other sensory modalities enter there

secondary sensory cortex vs somatosensory association area???

based on information that enters the sensory cortex, movement is initiated or continued by the…

more frontally situated premotor cortex

prefrontal association cortex (M3)?????

where motor action is planned on the basis of complex information from the sensory areas

signals conveyed from S3 to M3 are usually also influenced by the…

emotional limbic system

secondary motor cortex/supplementary motor area (M2)

• has to prepare movement in such a way that the correct muscle groups are used properly

• directly influences the spinal cord

• if the movements are already familiar through experience and practice, the brain can predict what will happen so it uses existing motor programmes = feedforward

• feedback is when a movement is initiated and then adjusted according to the result

basal ganglia

• basal nuclei/ganglion are located below the cortex on both sides of the hemispherical midline

• consist of the caudate nucleus, putamen and globus pallidus
  → caudate nucleus + putamen = the neostriatum/striatum
  → putamen + globus pallidus = the lenticular nucleus (lentiform nucleus)

• motor function of the basal nuclei together with the mesencephalon is regarded as separate from the pyramidal tract system = extrapyramidal system (but even though the cerebellum for example is situated outside the pyramidal tract system, it is not seen as part of the extrapyramidal system)

• motor function of young children is initially controlled by the extrapyramidal system, while myelination of the pyramidal tracts continues for years after birth

• occupy a key position because they receive input from virtually the entire cortex as well as the brainstem

  BUT the spinal cord does not directly send information to this system which means that the basal nuclei play only a minor role in external feedback from initiated movement

• As movement becomes less automatic and more planned, the prefrontal cortex (M3) and higher sensory areas (S2 and S3) increasingly come into play in motor function. The basal nuclei are also involved in this process, since they send information about planned voluntary movement from M3 to M2. A great deal of information is exchanged with M2, showing the control function of the basal nuclei

• associated with a variety of functions, including regulating voluntary motor movements, procedural learning, habit formation, conditional learning, eye movements, cognition and emotion

• supply M2 with existing practiced motor programmes and preparing those planned in M2 (?)

• also uses internal feedback with M2 → tests the scheme before the movement is initiated
  (cerebellum also uses internal feedback with M2 → assesses the efficiency of a motor function before movement is initiated)

• its dysfunction is seen in parkinsons

important pathways to and from the basal nuclei

Important pathways to and from the basal nuclei . Th thalamus, NC caudate nucleus , Pu putamen , S2 secondary sensory cortex , S3 tertiary sensory cortex , M2a supplementary motor cortex , M2b premotor cortex , M3 prefrontal cortex

motor function of young children is initially controlled by…

the extrapyramidal system, while myelination of the pyramidal tracts continues for years after birth

As movement becomes less automatic and more planned, the prefrontal cortex (M3) and higher sensory areas (S2 and S3) increasingly come into play in motor function. The basal nuclei are also involved in this process, since they send information about planned voluntary movement from M3 to M2. A great deal of information is exchanged with M2, showing the control function of the basal nuclei

the … and … have a ‘consultative function’ for M2

basal ganglia and cerebellum

statement: cerebellum → internal and external feedback among other things

direct and indirect pathways from the basal ganglia

think of these pathways are response systems (?) not pathways that directly cause motor movement

1. direct pathway

   • from the striatum to the globus pallidus then 2 pathways

     1. globus → substania nigra → thalamus

     2. globus → thalamus

     thalamus → motor cortex → spinal cord

   • activates/disinhibits the thalamus

2. indirect pathway

   • from the striatum via the globus pallidus (each doesnt synapse (?) there) to the subthalamic nucleus to the thalamus

     thalamus → motor cortex → spinal cord

   • photo doesnt make sense with ^

   • inhibits the thalamus

!! direct and indirect pathways thus have an opposite effect on motor function, and disorders causing motor defects can generally be explained in terms of an imbalance between these direct and indirect thalamocortical circuits

• eg. hyperkinetic disorders such as chorea can be explained as a relative overactivity of the disinhibiting direct system

• hypokinetic disorders such as parkinsonism are caused by relative overactivity of the inhibiting indirect system

• parkinson’s → malfunction of the dopaminergic cells in the substantia nigra (part of the direct pathway) causing degeneration of nigrostriatal pathways = direct system

  • sterotactic surgery can improve extrapyramidal motor disorders → the subthalamic nucleus is stimulated in patients with Parkinson’s disease , causing the indirect system to be inhibited

    wait so they stimulate the indirect system to INHIBIT it???

but not all motor defects right? only central ones

parkinson’s is a malfunction of the…

dopaminergic cells in the substantia nigra (part of the direct pathway) causing degeneration of nigrostriatal pathways = direct system

… surgery can improve extrapyramidal motor disorders

stereotactic surgery

eg. in parkinson, the subthalamic nucleus is stimulated in patients with Parkinson’s disease, causing the indirect system to be inhibited

all information from the basal nuclei to the cortex is transmitted via the…

thalamus

function of thalamus*****

descending motor pathways for posture and balance

• the rubrospinal, reticulospinal, vestibulospinal and tectospinal tracts are more under the influence of the basal nuclei (unlike the pyramidal tract) = bulbospinal pathways

• bulbospinal pathways → regulate axial and postural motor function and tone

• recall that a majority of the pyramidal tract (lateral) decussates and influences the distal musculature

  but a small part of it (anterior/medial) does not decussate, instead it branches off at its destination in the spinal cord and influences both sides of the body and mainly the proximal muscles of the trunk and limbs → responsible for posture and balance

• the rubrospinal tract is similar to the lateral pyramidal tract in terms of its anatomical course and function

• the other pathways are more similar to the medial pyramidal tract, and play an important role in axial and postural motor control

the red nucleus is…****

a part of the brain where the rubrospinal tract (only?) synapses at

tracts:

• afferent: corticorubral, cerebellorubral

• efferent: rubrospinal, rubroolivary tracts

which bulbospinal tract follows the same anatomical course and function as the lateral pyramidal tract

rubrospinal tract

does the pyramidal tract decussate

most of it (the lateral part) does, but the anterior/medial part doesnt

anterior/medial vs lateral pyramidal tract

recall that a majority of the pyramidal tract (lateral) decussates and influences the distal musculature

but a small part of it (anterior/medial) does not decussate, instead it branches off at its destination in the spinal cord and influences both sides of the body and mainly the proximal muscles of the trunk and limbs → responsible for posture and balance

symptoms in basal ganglia diseases

• defects in an extrapyramidal neuron circuit cause loss of function other than damage to the primary motor cortex and the pyramidal tract

• symptoms include too much (hyperkinesia, dyskinesia) or too little (hypokinesia) spontaneous movement, and difficulty initiating or sustaining movement (akinesia)

  but no paresis

• muscle tone is elevated but in a different way than in the case of CMN impairment, recall that it causes rigidity rather than spasticity

• problems with movement must be caused by defects in a subcortical circuit of the basal ganglia, whereas abnormal muscle tone is mainly caused by impaired output via the systems descending from the extrapyramidal system to the spinal cord

• unilateral defects → symptoms in the contralteral half of the body due to disturbance within the subcortical pathways between the cerebral cortex, basal ganglia and red nucleus

• proximal motor functions are influenced on both sides, in principle, due to the other descending tracts from the brainstem to the spinal cord that are influenced by the extrapyramidal system and have a bilateral influence on motor function

problems with movement vs abnormal muscle tone when it comes to the basal ganglia

problems with movement must be caused by defects in a subcortical circuit of the basal ganglia, whereas abnormal muscle tone is mainly caused by impaired output via the systems descending from the extrapyramidal system to the spinal cord

hyperkinesia**********

impairments affecting speed of movement and automaticity**********

hyperkinetic disorders

• = tremor, dystonia, myoclonus, chorea, tics etc

• can be (not always) caused by abnormalities in the basal nuclei

• tremor:

  • classified according to frequency, amplitude and the circumstances under which it occurs, eg.

    • unilateral resting tremor → consistent with Parkinson’s disease

    • bilateral action tremor→ consistent with essential tremor

    • tremor that increases as the target is approached → usually an intention tremor, consistent with a cerebellar disorder

• tics → divided into motor, phonic and sensory tics, and also categorized in terms of complexity, into simple and complex

• distribution and circumstances are also taken into account in myoclonus and chorea

  • eg. Sydenham’s chorea is located distally, whereas drug-induced chorea occurs in the face, trunk and arms, and chorea caused by Huntington’s disease is generalized

hypokinetic disorders

• hypokinesia or bradykinesia are important features of parkinsons (a hypO-KINETIC - hypER-TONIC disorder, ie hypertonia from rigidity)

• recall that extrapyramidal problems can cause rigidity

• impairment of the descending pathways from the brainstem (eg. in the cases of both spasticity and rigidity i think?) causes disinhibition not of the anterior horn cells but of the gamma motor neurons controlling the muscle spindles, which changes the muscle spindles’ point of reference (‘turns up the thermostat’), causing permanent hypertonia

  however, the symptoms of rigidity and spasticity are very different, check other flashcard

• parkinsons patients may experience substantial fluctuations, especially under the influence of medication

  there can be off states with hypokinesia and rigidity, and on states with hyperkinesia

• tremors in parkinson should not be regarded as hyperkinesia (because they actually dont occur during the off states with hypokinesia and rigidity)

• patients with parkinsons feel more comfortable with excessive movement (choreic), probably because these symptoms occur in a stage where the dopamine levels are relatively high and dopamine itself has a positive effect on cognitive symptoms and mood

tremors in parkinson should not be regarded as…

hyperkinesia (because they actually dont occur during the off states with hypokinesia and rigidity)

why do patients with parkinsons feel more comfortable with excessive movement (choreic)

probably because these symptoms occur in a stage where the dopamine levels are relatively high and dopamine itself has a positive effect on cognitive symptoms and mood

parkinsons patients may experience…

substantial fluctuations, especially under the influence of medication

there can be off states with hypokinesia and rigidity, and on states with hyperkinesia

rigidity vs spasticity

rigidity → extrapyramidal, velocity independent, affects both the agonist and antagonist muscles, plantar reflex and tendon reflexes are usually normal

(spasticity generally occurs only during muscle stretch)

WHY IS THERE A TIC (HYPERKINETIC) IN PARKINSONS WHEN ITS A HYPOKINETIC DISORDER

froments sign in rigidity????****

cerebellum functional anatomy

• function = balanced execution

• do not fucking confuse with the cerebrum (= majority of the brain, the part that has the cerebral cortex)

• part of a feedback system

  ie. planned movement is checked and adjusted by the cerebellum prior to (internal feedback) and during its execution (external feedback)

• since its involved in both internal and external feedback, it receives information from the vestibular nuclei, contralateral cerebral cortex (M2) and from the ipsilateral spinal cord via the spinocerebellar tract

• notice how it gets info from the contralateral cerebral cortex but the ipsilateral spinal cord

  this is because the left cerebellum controls the left half of the body

• divided into 3 parts

  1. spinocerebellum

     • = vermis (proximal motor function) + medial parts of the hemispheres (distal motor function)

     • receives information directly from the spinal cord → can control a movement once it has been initiated

     • feedback to the IPSILATERAL spinal cord is given via the the CONTRALATERAL red nucleus
       also from the rubrospinal tract and contralateral cerebral cortex

  2. cerebrocerebellum

     • = compromises the 2 cerebellar hemispheres

     • is in contact with the contralateral cortex via the corticopontine pathways

     • involved in the planning of future movement (internal feedback)

     • receives information for the direct control of initiated movement from the corticospinal tract as it travels to the spinal cord via the pontine nuclei

     • this info goes back to the cortex via the contralateral thalamus

  3. vestivulocerebellum

     • = flocculonodular lobe

     • completely situated within the cerebellum

     • controls balance and ocular motor function

cerebellar symptoms

• main symptom = axatia = lack of coordinated movement in the absence of muscle weakness → excessive movement that can overshoot OR compensatory movements that do not end in time (disturbed rebound phenomenon)

• attempts to compensate for ataxia also fail due to the lack of coordinated movement, leading to cerebellar tremor, especially when approaching a target = intention tremor

• antagonistic movements become too large and clumsy + slow

• acute stage, patients with cerebellar ataxia complain of dizziness, but that clears up quickly and they then feel unsure of their footing

• these were the general symptoms but it can also differ according to where in the cerebellum it exactly is, eg.

  • hemispheric syndrome → ipsilateral ataxia of the arm and leg

  • caudal vermis → trunk ataxia with normal limb coordination

• saccade dysmetria = eyes do not move smoothly

• hypermetria eyes overshoot their intended target

• nystagmus (since part of the cerebellum control oculomotor movement***)

• might fall back into a chair after getting up and letting go of the chair arm due to truncal ataxia

• while turning, a cerebellar disorder may cause the moving leg to swing outwards (i think the book is wrong, circumduction is more for pyramidal diseases ie. paresis while overshooting the step ie. hypermetria is for cerebellar)

what is the main symptom of cerebellar dysfunction

ataxia (usually upper limb)

other than movement, the basal ganglia and cerebellum also affect…

basal ganglia are not only connected with the motor cortical regions but also with the prefrontal association areas and the limbic system = links ‘motion’ and ‘emotion’

the cerebellum plays a role in cognitive processes and cognitive development. The mind and motor function are therefore more interconnected than was long thought

examination of central motor control - central motor function tests***

^a extrapyramidal disorder ,

^b pyramidal system disorder ,

^c cerebellar disorder and

^d epicritic system disorder.

examination of central motor control - main forms of dysarthria (motor speech disorder)***

Impaired speech can be caused by impaired motor function (central or peripheral) or impaired motor control (cerebellar or extrapyramidal)

parkinsons disease symptoms general

• facial hypomimia = stolid facial expression

• reduced blinking frequency

• abnormal posture

• during finger tapping (tapping the thumb and index together for 30s) they generally exhibit a progressive decrease in the amplitude of the movements and become hesitant

• often find it hard to get up from a chair

• arm swings may be less pronounced in one or both arms in the early stages

hyperkinetic syndromes

characterised by facial tics → rapid blinking, winking, raising eyelids or a corner of the mouth and sometimes tongue protrusion

dystonia

may be accompanied by excessive closure of (usually both) eyes and an abnormal contraction of a corner of the mouth

position of the head may be abnormal

• torticollis = head tilted to one side (usually slightly backwards)

• antecollis = forward hyperextension

• retrocollis = backward hyperextension

pyramidal tract involvement often causes…

asymmetry in the lower half of the face

how does the cerebellum affect eye movements

eyes do not move smoothly but jump around (saccade dysmetria) and overshoot their intended target ( hypermetria ). Often nystagmus occurs when the patient is instructed to look at a stationary finger held 45 degrees to the side of the face. The eyes will then simultaneously saccade in the direction of the fixated object. Nystagmus can be interpreted as an intention tremor of the gaze.

how are eye movements affected in extrapyramidal impairment

• field of vision in the vertical plane may be restricted, particularly in the downward direction = progressive supranuclear paresis

• dyskinesia can cause oculogyric crisis = upward or downward deviation of the eyes

• several hypokinetic syndromes make it hard for patients to quickly shift their gaze, eye movements are generally slow or interrupted

actual question: does extrapyramidal impairment cause hypo or hyperkinetic???

upper limb ataxia

• cerebellar impairments often cause ataxic symptoms in the arms

• check for any intention tremors, especially during the finger-to-nose test

• the target will only be missed if the ataxia is severe

  If the ataxia is mild and the nose is still missed with eyes open or closed, this should be regarded as a functional neurological phenomenon

• recall from theme 1 that if the test can be completed w/ eyes open but not closed then deep sensation is impaired (sensory ataxia)

• finger to finger test is more sensitive than finger to nose test

• although these tests can be done smoothly by a patient w/ extrapyramidal syndrome, they will be slower

• in the case of both cerebellar and extrapyramidal disorders (also CMN impairment) tests involving antagonistic movements (diadochokinesis) will be positive → eg. switching between supination and pronation, rapid finger movements

  isnt the cerebellum part of the extrapyramidal tract??? no it isnt they literally stated that

• in parkinson’s patients, during finger tapping (tapping the thumb and index together for 30s) they generally exhibit a progressive decrease in the amplitude of the movements and become hesitant

• in cerebellar disorders, when trying to grasp something between the thumn and index finger they will make the gap too wide and overshoot the object

  • also rotations in the wrist will be too large and irregular

  • also a rebound phenomenon occurs = unable to correct the position of a limb

  • handwriting → irregular letters, abnormally large letters (macrographia) and untidy handwriting

• in extrapyramidal syndromes, the ranges of motion are too small and slow

  • also unlike cerebellar disorders, this causes abnormally small handwriting (micrographia)

diadochokinesis

the inability to perform rapid alternating muscle movements

actual q: why does it not count as ataxia if they also cant touch their nose with their finger if there eyes are open???

components of the extrapyramidal system

The main components of the extrapyramidal motor system are the nuclei of the basal ganglia. Other structures which are involved include the nuclei of the cerebellum and brainstem, as well as the mesencephalic reticular formation

lower limb ataxia

• can be detected by observing gait and heel-to-shin

• heel-to-shin → patient is instructed to smoothly place a heel on the knee of the other leg, wait for a second and then smoothly move the heel along the edge of the tibia to the great toe

  • cerebellar disorder → will overshoot the knee (hypermetria) and there will be an intention tremor → movement will be jerky and the heel will lose contact with the shin

  • those with sensory ataxia will benefit from visual correction

• cerebellar leg ataxia also manifests itself during walking as the patient exhibits too much hip flexion and swings the leg too far forward = hypermetria

truncal movements***

Patients with Parkinson’s disease often find it hard to get up from a chair. They do not automatically move their feet backwards and push themselves up with their hands. Sometimes they have to make a few attempts, falling back into the chair when unsuccessful.

When letting go of the arm the patient may fall backward; in severe cerebellar disorders the patient may not be able to sit unaided because of truncal ataxia. In less severe disorders the rebound of the trunk may be impaired when that of the arms is tested: the patient falls backwards when the arm is released

muscle tone

• can be tested by inducing slow passive movement across joints

• extrapyramidal problem → resting muscle tone is usually elevated across the entire range of motion and cogwheel rigidity is often present

  + activation of other muscle groups may show rigidity sooner

• CMN involvement → spasticity

• cerebellar → can cause hypotonia

activation of …. may show rigidity sooner

other muscle groups

muscle stretch reflexes

• normal in extrapyramidal impairment

• cerebellar → the patellar reflex test may produce pendular reflexes: the lower leg keeps swinging for a while because the movement is not inhibited

  low significant tho

• CMN → hyperreflexia and babinski

muscle stretch reflexes are… in extrapyramidal impairment

normal

gait and stance

• even minor CMN problems can cause impairment of postural reflexes

  • test by instructing the patient to stand erect with their feet together or as close as possible

    if the patient does not sway in this position, start the push and pull test = gentle pushes in various directions

  • romberg tests deep sensation which is NORMAL in cerebellar disorders

    suddenly falling or losing one’s balance after closing the eyes will usually be due to a functional neurological disorder

• the types of atasis (insecure standing) and abasia (insecure walking) depend on where the lesion is (CHECK PHOTO)

• a heel to toe test just tells you if the CNS is functioning normally

  if abnormalities are found then a more detailed examination is needed

• while turning, a cerebellar disorder may cause the moving leg to swing outwards

• arm swings may be less pronounced in one or both arms in the early stages of parkinson’s

while turning, a cerebellar disorder may cause

the moving leg to swing outwards

figure 5.7!!!!!!!!!!!!!

cerebellar function tests are abnormal in … and … (not disorders)

children below age 12 and the sense of balance declines with age

also standing and walking become harder when people are nervous

those with functional neurological disorders often perform better on … than on …

often perform better on difficult tests than on simple ones and distraction leads to better results

chapter 5 key points

• In the case of basal ganglia dysfunction, voluntary movements are often restricted, and in the case of a cerebellar problem they will be too large.

• An extrapyramidal disorder can be accompanied by hypokinesia or sometimes hyperkinesia.

• Tremors due to basal ganglia dysfunction are linked to hypokinesia.

• The increase in tonus in a patient with impaired basal ganglia is different from that in one with spasticity, namely greater stiffness throughout the range of motion with no ‘give’, i.e. rigidity.

• The basal ganglia communicate with the ipsilateral cortex, the cerebellum with the contralateral cortex

chapter 8 key points

• A number of higher functions can be localized, but even they can be impaired due to a problem further on that impedes the supply of information.

• The functions related to perception are located in the posterior part of the cerebrum, those involving action in the anterior part.

• In 95 % of people, the language-dominant hemisphere is the left one (that includes half of left-handed people), and it is the seat of mainly analytical functions.

• The non-language-dominant hemisphere is no less important, being the seat of emotion, strategic understanding and spatial understanding in particular.

• Aphasia can broadly be divided into receptive and expressive aphasia, but both of these elements are usually somewhat impaired in a patient with aphasia. There are also some specific types of aphasia.

• Apraxia is the inability to act and is used in various contexts – sometimes wrongly. The performance of actions on command or according to an internal plan originates mainly in the language-dominant hemisphere, even if the non-dominant hand is being used.

• Agnosia can take on fairly complex forms. The patient perceives something but fails to recognize it. This is almost always due to an impaired connection between two cortical areas (disconnection).

• Speech is altered also as a result of problems in the non-language-dominant hemisphere: it is less musical, more monotonous (aprosodia). The patient understands factual matters but misses emotional undertones, which can lead to distressing misunderstandings.

• Spatial disorders are caused by problems in the posterior parts of the non-language-dominant hemisphere. A particular type is problems with dressing, referred to – not entirely correctly – as ‘dressing apraxia’.

• Vitamin B ₁ deficiency causes severe types of short-term memory disorders, Korsakoff’s syndrome. These are often due to an alcohol problem, but not always.

• Transient global amnesia – as far as we know – is a harmless syndrome that does not require any additional tests.

• There are two sides to a frontal syndrome: (a) insufficient activity (orbitofrontal) and (b) disinhibition of action and omission (dorsolateral). The patient has no overview and behaves chaotically.

• As the posterior cerebral artery supplies part of the hippocampus, infarctions in the posterior cortex can also cause mental phenomena.

• Various neurological (especially degenerative) disorders are accompanied by altered consciousness (delusions, hallucinations).

• The MMSE and the Frontal Assessment Battery can be used to test the higher functions: these tests are complementary. The MoCA test lies between the two and is essentially a combination of both.

diffuse and local cortical disorders

1. dementia → deterioration in cognitive funtcion due to general neuron loss

if its local loss, the following may occur:

1. aphasia → language disorders

2. apraxia → inability to perform purposive actions

3. agnosia → inability to interpret sensory information

the presence of a cognitive disorder can only be established if…

primary motor and sensory capability, consciousness and cooperation are all reasonably normal

eg. aphasia cannot be diagnosed if they have a motor disorder that prevents normal speech, apraxia cannot be diagnosed if hemiplegia is present in the same half, and astereognosis (agnosia) is identifiable only if primary tactile sensation is normal

insular***

anatomy of the cerebrum

• consists of 2 cerebral hemispheres separated by the falx cerebri of the dura mater

• rear part = parietal, temporal and occipital lobes → involved in mainly perception and secondarily the initiation of action

• Front part = frontal lobes → important for executive functions and the integreert of personality

• Perception has 3 stages → information is input (= primary cortical zone), analysed (= secondary cortical zone) and then put into context (tertiary cortical zone)

• Secondary areas are also known as association areas

  But each area deals with one sensory quality so they’re described as unimodal, several unimodal association areas form a heteromodal association area = tertiary cortex ????? How does that make sense

  is it like the stimuli from the unimodal association areas combine in the heteromodal association area/tertiary cortex to form a single concept

• The synthesis of information can lead the prefrontal cortex to initiate a voluntary action

• The secondary cortical regions (where gnostic sensory info is processed in order to locate things in space = ‘where’) have fairly direct connections to the secondary motor regions

• The info comes in → primary cortex → secondary cortex/unimodal association areas process info in order to locate things in space (where) → all info combines in the heteromodal tertiary cortex, sends all information about ‘what’ to → Limbic cortex

  ‘what’ information can also be relayed via the protopathic system

  wait idk if ^is true? is it where → what → limbic? or where AND what → limbic

  The secondary cortical regions, in which gnostic sensory information is processed in order to locate things in space (‘where’), have fairly direct connections to the secondary motor regions (fig.  5.​1-M2) where movements are generated. The sensory information related to the nature of ‘what’ is relayed via the heteromodal areas, after being linked to other information, to the limbic cortex (fig.  8.2). A substantial amount of information on the sensory ‘what’, especially that relating to emotion, is also relayed via the protopathic system (sect.  4.​1.​6). There is a similar division into ‘where’ and ‘what’ (see sect.  9.​1.​2) in the case of the other modalities, but slightly different in each case.

which cortical hemisphere is language dominant

left (usually… roughly 90% of people are right handed, for them language is usually on the left)

• left also deals w/ musical analytical capability and the sense of rhythm

right (in 95% of people) is more associated with feeling, expressing and perceiving emotion AND emotional language use such as prosody (= sentence melody, emotional hue of language) and intonation

• also regulates attention, visual spatial perception, orientation in the left half of the body and the recognition or evaluation of melodies

where is hemispherical specialisation less pronounced

in the medial regions of the hemispheres

this is where the phylogenetically old (paleocortex = blue) and new (neocortex = grey) parts of the cortex meet in the mesial temporal cortex (medial temporal lobe)

the limbic region is = ?

paleocortex + boundary area (what like the mesial temporal cortex?)

the limbic system has close connections to the…

hypothalamus and the olfactory area, which is why the limbic system can influencing the:

1. autonomic NS, eg. → goose-bumps triggered by a thought

2. endocrine system, eg. → perceiving and responding to sexual stimuli

emotion and memory

• regulated by the primary limbic system

  • components → the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus

• amygdala function → to establish the emotional and motivational value of incoming sensory information

  • since its connected to the hypothalamus, it means that the autonomous NS is triggered by the emotional cues

  • if it were able to function entirely unchecked, every stimulus would initiate a strong impulsive response but it is inhibited by the frontobasal cortex → enables the adaptation of impulsive behaviour

  • however, a stimulus that is not immediately recognized can elicit a strong impulse response

• the hippocampus is also located close to the amygdala → plays a central role in memory formation and therefore temporal orientation (measurement of memory?)

  The amygdala processes incoming information from the sensory association areas (fig.  8.1-9) and attaches (often persistent) emotional significance to it (supplementary response by the amygdala). Memories are not retained in the hippocampus for long, however. Instead, the processed data is returned to the cortex regions that the ‘raw’ information came from. Thus, if similar information is perceived again in the future, appropriate associations can quickly be made, so that something may be immediately recognized as ‘nice’, ‘frightening’, or ‘horrid

• i think ^ is like the hippo keeps getting short term and changes them into long term associated with somethin else an sends them to be stored elsewhere?

https://thebrain.mcgill.ca/flash/d/d_07/d_07_cr/d_07_cr_tra/d_07_cr_tra.html

what inhibits the amygdala

frontobasal cortex

… is the part of the brain involved when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses

limbic system

8.1.5???***

aphasia

• can occur in isolation but is usually accompanied by a loss of the ability to read (alexia) and write (agraphia) and quire often by motor disorders affecting one half of the body (usually the dominant side)

• can be loosely split into mainly expressive and mainly receptive disorders, this is based mainly on the ability to speak easily and articulately (fluency)

  1. motor aphasia = mainly expressive/fluent lesion:

     • usually localised towards the front of the posterior frontal cortex (of the dominant hemisphere), specifically in the inferior frontal gyrus/brocas speech centre = broca’s aphasia

     • able to understand language but cannot put thoughts into words (not adequately)

     • starting to speak is hard, speech is slow and full of pauses, right word is hard to find, words get muddled up, repetition is frequent

     • letters or letter groups are often revered = literal paraphasia

     • preference for nouns

     • patient is aware of their inability to express themselves normally → liable to become distraught or angry

  2. sensory aphasia = mainly receptive/non fluent lesion:

     • usually localised towards the back of the dominant hemisphere = temporal lobe, specifically in the superior temporal gyrus/wernicke’s speech centre

     • ag. wernicke’s aphasia

     • also known as jargon aphasia

     • understanding of language is seriously impaired

     • patient can speak (often fast w/ normal intonation) but construction of sentences is incomplete using fixed phrases and sometimes joins unrelated separate words together

     • preference for verbs and adjectives

     • words are used in the wrong sense (semantic paraphasia) or completely new words are formed (neologisms)

     • if serious → loses ability to read and write

     • if mild → reading ability is normal but they dont understand

     • usually unaware that anything is wrong and its hard to communicate with them

  other forms

  3. amnestic aphasia/anomia:

     • characterised mainly by difficulty remembering names and words in isolation

     • not always so obvious in spont. speech (typ. fluent) but recognisable if the patient is asked to name a series of objects or images

     • location of lesion is variable

  4. conduction aphasia:

     • disorders of the arcuate fasciculus which connects the temporal and frontal language areas

     • unable to repeat a sentence, mild problems with findinf the right word + mild literal paraphasia

     • spont. speech is largely normal and comprehension is good but reading aloud and writing are impaired

  5. transcortical aphasia:

     • transcortical motor aphasia → unable to form a complete sentence in answer to a question

     • transcortical sensory aphasia → unlike ^, complete answers can be formed but with lots of semantic paraphasias (when an entire word is substituted for the intended word)

     • ability to repeat is normal

  6. mixed (possibly total) aphasia:

     • most common form

     • both expressive and receptive forms are expressed but one form may be more pronounced

     • usually due to extensive lesions or to deep-lying lesions that disrupt the pathways between the cortical speech areas

what is the most common type of aphasia

mixed

if aphasia is due to …, partial or even total recovery is possible

a non-progressive cerebral problem (cerebral infarction, traumatic brain injury)

gerstamann’s syndrome

a neuropsychological disorder characterised by:

1. agraphia (inability to write)

2. acalculia (inability to perform mathematical calculations)

3. finger agnosia (inability to name, discriminate, or identify fingers)

4. left-right disorientation (inability to distinguish left from right)

• due to a problem in the posterior region of the angular gyrus

• combo of symptoms is due to a problem in spatial awareness

apraxia

• inability to perform purposive actions (despite having an intact plan of action) or make gestures, although there is no motor disorder and the instruction is understood

• caused by a problem in the language-dominant hemisphere, but affects both hands (eg. if a R handed patient has a L hemisphere problem, they may also lose the ability to do things w/ both their L and R hands)

  → specifically in the inferior parietal gyrus

  → can also be a due to a problem in the connection between the inferior parietal gyrus and the secondary motor regions (!! the inferior parietal gyru is connected to the contralateral secondary motor region, so an injury in that connection can only cause CONTRALATERAL ideomotor apraxia)

• ideomotor apraxia = inability to voluntarily perform a learned task when given the necessary objects (eg. if given a screwdriver, the may try to write with it)

• mild cases → appear slightly clumsy or absent minded, ability to copy actions may be retained but instructions cannot be followed

• ideational apraxia = only spontaneous action (making coffee, unwrapping a present) is impaired, or the patient is unable to follow instructions only when a series of actions is involved (which require a plan of action)

the term apraxia is also sometimes used to refer to problems of performing activities controlled from other parts of the brain

1. micturition apraxia and gait apraxia → attributable to problems in the deep frontal cortex

2. dressing apraxia and constructive apraxia (arise in the non dominant hemisphere)

3. apraxia of lid opening

4. verbal apraxia and buccofacial apraxia → often caused by injury to broca’s speech centre or a nearby area

   typically accompanied by non fluent aphasia

agnosia

• = inability to recognise and integrate sensory perceptions

• diagnosis is only appropriate if the peripheral apparatus is reasonable intact (eg. it cant be visual agnosia if their eyesight is defective)

• tactile agnosia:

  • due to lesions in the parietal lobe close to the primary sensory cortex

    contralateral to the lesion its undetected or only in the test???

  • main symptoms is astereognosis = inability to recognise objects by touch

  • often aware of pain or tactile stimuli but cant accurately localise the source

  • A good way to test for tactile agnosia is to provide simultaneous, symmetrical stimuli to both halves of the body. Contralateral to the lesion, the stimulus will be undetected, even though the patient is able to discern the stimuli individually, because attention in the affected hemisphere is extinguished by attention in the healthy hemisphere = tactile extinction

• anosognsoia = being unaware that one half of the body is dysfunction

  occurs in cases of acute (usually vascular) injury to the non dominant parietal cortex, usually disappears after a few hours or days (the injury or being unaware???)

• body scheme disorder???

• autotopagnosia = inability to recognise and name parts of the one’s own body, likely to be due to a problem in the language-dominant hemisphere

  eg. finger agnosia

  → regarded as part of a naming disorder

• visual and acoustic agnosia → stimulus is perceived but not understood = sensory information is not correctly associated with other retained information in the heteromodal tertiary association areas (eg. will hear the sound of a bunch of keys being rattled, but identify the sound as falling marbles)

kluver-bucy syndrome

• very rare form of agnosia

• due to the limbic system not receiving the correct information or is deactivated (sensory limbic disconnection) → no emotional significant is attached to incoming stimuli, oral tendency, hypersexuality, memory loss, failure to recognise familiar objects and people (visual agnosia and prosopagnosia respectively), loss of fear and abnormal aggression (last 2 are due to disconnection of the amygdala)

• = bilateral dysfunction of the frontal region of the temporal lobe (thats where the limbic system is right???), usually most pronounced on the right

• can develop after bilateral neurosurgical procedures or an infection such as herpes simplex encephalitis, in the context of a degenerative syndrome such as frontotemporal dementia or following a traumatic brain injury or CVA

aprosody

• = inability to recognise or produce affective vocal inflection or facial expressions of emotion

• diagnosis is important to prevent patients with injuries to the non-dominant hemisphere from being perceived as dissatisfied or ill-tempered

cognitive symptoms that are lesions in the language vs non language dominant cortex

spatial disorders

• due to problems in the posterior regions of the non dominant hemisphere

• characterised by the inability to depict spatial relationships when copying or drawing

• often accompanied by dressing apraxia

• If a disorder in the posterior of the non-dominant hemisphere is suspected, confirmation can be sought by asking whether the patient often has problems finding their way when out and about in familiar places or even when at home ( topographical disorientation ), or is apt to forget the whereabouts of things they have put away